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Iron Deficiency Anemia

Why elevated Ferritin excludes IDA? What about inflammatory State?

Ali Fadhil

on 15 May 2013

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Transcript of Iron Deficiency Anemia

Well, rarely... Your patient will complain "my legs are weak and I feel no energy." IDA can cause generalized fatigue, it is not a myth. 0 Irron defeciency from concept to company on EXAM what is this? Can IDA kill
you? Team
A Workup My Labs Signs and Symptoms Hypoxic deaths have been observed in patients who refuse blood transfusions for religious reasons. Whereas a number of symptoms, such as ice chewing and leg cramps, occur with iron deficiency, the major debility of moderately severe iron deficiency is fatigue and muscular dysfunction that impairs muscular work performance. # Ali Fadhil @ Atlanta Medical Center 2013 Iron deficiency anemia develops when body stores of iron drop too low to support normal red blood cell (RBC) production.

Inadequate dietary iron, iron absorption, bleeding, or loss of body iron in the urine may be the cause. One To The World Iron Defeciency Anemia IMS-A Fatigue and diminished capability to perform hard labor
Leg cramps on climbing stairs
Craving ice (in some cases, cold celery or other cold vegetables) to suck or chew
Poor scholastic performance
Cold intolerance
Reduced resistance to infection
Altered behavior (eg, attention deficit disorder)
Dysphagia with solid foods (from esophageal webbing)
Worsened symptoms of comorbid cardiac or pulmonary disease Pallor of the mucous membranes (a nonspecific finding)
Spoon-shaped nails (koilonychia)
Fissures at the corners of the mouth (angular stomatitis)
A glossy tongue, with atrophy of the lingual papillae
Splenomegaly (in severe, persistent, untreated cases)
Pseudotumor cerebri (a rare finding in severe cases) Anemia of chronic disorders
Hemoglobin CC disease
Hemoglobin DD disease
Lead poisoning
Microcytic anemias
Autoimmune hemolytic anemia
Hemoglobin S-beta thalassemia DDx: Sideroblastic Anemias
Spherocytosis, Hereditary
Thalassemia, Alpha
Thalassemia, Beta IDA could be inferred from H&P but it is primarily a laboratory diagnosis.
Perform CBCs, peripheral blood smears.
and iron studies: serum iron, total iron-binding capacity [TIBC], ferritin, saturation percentage.
Useful tests include a complete blood count (CBC); a peripheral smear; serum iron, total iron-binding capacity (TIBC), and serum ferritin; evaluation for hemosiderinuria, hemoglobinuria, and pulmonary hemosiderosis; hemoglobin electrophoresis and measurement of hemoglobin A2 and fetal hemoglobin; and reticulocyte hemoglobin content. Other laboratory tests (eg, stool testing, incubated osmotic fragility testing, measurement of lead in tissue, and bone marrow aspiration). CBC: helps in documenting the severity of the anemia. In chronic IDA the cellular indicies show microcytic hypochromic RBCs with both MCV and MCHC low. the platelet count is elevated (>450,000/L); this elevation normalizes after iron therapy. Peripheral Smear:
Very important part of the workup. Can detect microcytosis long before MCV goes below normal value. Iron level, TIBC, Ferritin: Plasma iron bound to transferrin — 3 to 7 mg.
The remainder is storage iron in the form of ferritin or hemosiderin. Storage iron in adult men has been estimated as being approximately 10 mg/kg, and is found mostly in liver, spleen, and bone marrow Adult women have less storage iron, depending upon the extent of menses, pregnancies, deliveries, lactation, and iron intake. Let's start with a question: why elevated Ferritin eleminates IDA? Does it? Iron stores (mg) ≈ (8 to 10) x ferritin (ng/mL) Serum FERRITIN and the inflammatory State: Ferritin is an acute phase reactant, with plasma levels increasing in liver disease, infection, inflammation, and malignancy.
Thus, a patient with iron deficiency and a concomitant inflammatory disease such as rheumatoid arthritis may have a "falsely" normal ferritin concentration.
The effect of inflammation is to elevate serum ferritin approximately threefold.
A useful rule-of-thumb in such patients is to divide the patient's serum ferritin concentration by three; a resulting value of 20 or less (ie, an initial serum ferritin <60 ng/mL) suggests concomitant iron deficiency.$$
The accuracy of measurement of transferrin/TIBC for predicting the presence of iron deficiency is second only to the serum or plasma ferritin concentration. Low serum iron and ferritin levels with an elevated TIBC are diagnostic of iron deficiency.
While a low serum ferritin is virtually diagnostic of iron deficiency, a normal serum ferritin can be seen in patients who are deficient in iron and have coexistent diseases (eg, hepatitis or anemia of chronic disorders). Pica and pagophagia
Restless legs syndrome: Rx with Iron Serum ferritin: The serum or plasma ferritin concentration is an excellent indicator of iron stores and has replaced assessment of bone marrow iron stores as the gold standard for the diagnosis of IDA.
The ferritin concentration ranges from 40 to 200 ng/mL (mcg/L) in normal subjects, and is markedly elevated in states of iron overload.
There is no clinical situation other than iron deficiency in which extremely low values of serum ferritin are seen.
virtually all patients with serum ferritin concentrations less than 10 to 15 ng/mL are iron deficient, with a sensitivity of 59 percent and a specificity of 99 percent.
a cutoff limit of 41 ng/mL for serum ferritin provides improved diagnostic efficiency, with a sensitivity and specificity of 98 and 98 percent, respectively. Iron stores (mg) = (8 to 10) x ferritin (ng/mL) Remember this: Total Iron Stores= 4000mg Therefore, it is probably inappropriate to say there is IDA when ferriting is elevated >___ $$--Serum ferritin is often ordered to assess whether the patient is iron sufficient, rather than deficient. Using bone marrow iron stores as a gold standard, a study of 259 anemic patients over the age of 65 concluded that, in populations with a prevalence of iron deficiency of less than 40 percent, values of serum ferritin >100 mcg/L reduce the probability of iron deficiency to under 10%. The sequence of events (left to right) that occur with gradual depletion of body stores of iron. Serum ferritin and stainable iron in tissue stores are the most sensitive laboratory indicators of mild iron deficiency and are particularly useful in differentiating iron deficiency from the anemia of chronic disorders. The percentage saturation of transferrin with iron and free erythrocyte protoporphyrin values do not become abnormal until tissue stores are depleted of iron. Subsequently, a decrease in the hemoglobin concentration occurs because iron is unavailable for heme synthesis. Red blood cell indices do not become abnormal for several months after tissue stores are depleted of iron. Sequential changes in laboratory values following blood loss are depicted. A healthy human was bled 5 L in 500-mL increments over 45 days. A moderate anemia ensued, initially with normal cellular indices and serum iron. Subsequently, the mean corpuscular volume (MCV) increased as iron was mobilized from body stores and reticulocytosis occurred. The serum iron decreased, followed by an increase in the total iron-binding capacity. Gradual decreases in the red blood cell indices occurred, with maximal microcytosis and hypochromia present 120 days after bleeding. Values returned to normal approximately 250 days after blood loss. At the end of the experiment, iron was absent from body stores (marrow) because hemoglobin has a first priority for iron. Iron-59 absorption was increased after all values returned to normal in order to replenish the body store with iron. This suggests that the serum iron, total iron-binding capacity, hemoglobin concentration, and indices were not the primary regulators of iron absorption. The total body iron in a 70-kg man is about 4 g. This is maintained by a balance between absorption and body losses. Although the body only absorbs 1 mg daily to maintain equilibrium, the internal requirement for iron is greater (20-25 mg). An erythrocyte has a lifespan of 120 days so that 0.8% of red blood cells are destroyed and replaced each day. A man with 5 L of blood volume has 2.5 g of iron incorporated into the hemoglobin, with a daily turnover of 20 mg for hemoglobin synthesis and degradation and another 5 mg for other requirements. Most of this iron passes through the plasma for reutilization. Iron in excess of these requirements is deposited in body stores as ferritin or hemosiderin. Peripheral blood smear in iron deficiency anemia. The enlarged central area of pallor in the red blood cell (arrows) indicates a decrease in hemoglobin synthesis, which is characteristic of the microcytic anemias. The mean corpuscular hemoglobin concentration is decreased.(From Wickramasinghe SE, McCullough J: Blood and Bone Marrow Pathology. Philadelphia, Churchill Livingstone, 2003, Fig. 11-6.) Only exception is when patient have sever liver disease such as hepatitis (eg. Autoimmune) then IDA could coexist with Ferritin in the thousands.
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